Long-term exposure to ambient ozone and mortality: a quantitative systematic review and meta-analysis of evidence from cohort studies.
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ABSTRACT:
SUBMITTER: Atkinson RW
PROVIDER: S-EPMC4769417 | biostudies-other | 2016 Feb
REPOSITORIES: biostudies-other
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Project description:Long-term ozone (O3) exposure may lead to non-communicable diseases and increase mortality risk. However, cohort-based studies are relatively rare, and inconsistent exposure metrics impair the credibility of epidemiological evidence synthetization. To provide more accurate meta-estimations, this study updates existing systematic reviews by including recent studies and summarizing the quantitative associations between O3 exposure and cause-specific mortality risks, based on unified exposure metrics. Cross-metric conversion factors were estimated linearly by decadal observations during 1990-2019. The Hunter-Schmidt random-effects estimator was applied to pool the relative risks. A total of 25 studies involving 226,453,067 participants (14 unique cohorts covering 99,855,611 participants) were included in the systematic review. After linearly unifying the inconsistent O3 exposure metrics , the pooled relative risks associated with every 10 nmol mol-1 (ppbV) incremental O3 exposure, by mean of the warm-season daily maximum 8-h average metric, were as follows: 1.014 with 95% confidence interval (CI) ranging 1.009-1.019 for all-cause mortality; 1.025 (95% CI: 1.010-1.040) for respiratory mortality; 1.056 (95% CI: 1.029-1.084) for COPD mortality; 1.019 (95% CI: 1.004-1.035) for cardiovascular mortality; and 1.074 (95% CI: 1.054-1.093) for congestive heart failure mortality. Insignificant mortality risk associations were found for ischemic heart disease, cerebrovascular diseases, and lung cancer. Adjustment for exposure metrics laid a solid foundation for multi-study meta-analysis, and widening coverage of surface O3 observations is expected to strengthen the cross-metric conversion in the future. Ever-growing numbers of epidemiological studies supported the evidence for considerable cardiopulmonary hazards and all-cause mortality risks from long-term O3 exposure. However, evidence of long-term O3 exposure-associated health effects was still scarce, so more relevant studies are needed to cover more populations with regional diversity.
| S-EPMC9065904 | biostudies-literature
Project description:Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.
| S-EPMC4105969 | biostudies-literature
Project description:Chronic obstructive pulmonary disease (COPD) is the third leading cause of death globally and ozone exposure is a main cause of its disease burden. However, studies on COPD hospitalizations from short-term ambient level ozone exposure have not generated consensus results. To address the knowledge gap, comprehensive and systematic searches in several databases were conducted using specific keywords for publications up to February 14, 2020. Random-effect models were used to derive overall excess risk estimates between short-term ambient-level ozone exposure and COPD hospitalizations. The influence analyses were used to test the robustness of the results. Both meta-regression and subgroup analyses were used to explore the sources of heterogeneity and potential modifying factors. Based on the results from 26 eligible studies, the random-effect model analyses show that a 10 µg/m3 increase in maximum 8-h ozone concentration was associated with 0.84% (95% CI: 0.09%, 1.59%) higher COPD hospitalizations. The estimates were higher for warm season and multiple-day lag but lower for old populations. Results from subgroup analyses also indicate a multiple-day lag trend and bigger significant health effects during longer day intervals. Although characteristics of individual studies added modest heterogeneity to the overall estimates, the results remained robust during further analyses and exhibited no evidence of publication bias. Our systematic review and meta-analysis indicate that short-term ambient level ozone exposure was associated with increased risk of COPD hospitalizations. The significant association with multiple-day lag trend indicates that a multiple-day exposure metric should be considered for establishing ambient ozone quality and exposure standards for improvement of population health. Future investigations and meta-analysis studies should include clinical studies as well as more careful lag selection protocol.
| S-EPMC7143242 | biostudies-literature
Project description:IntroductionThe health effects of ambient ozone have been investigated in many previous studies. However, the effects of long-term exposure to ambient ozone on the incidence of cardiovascular disease (CVD) remain inconclusive.ObjectivesTo estimate the associations of long-term exposure to maximum daily 8-hours average ozone (MDA8 O3) with the incidence of total CVD, heart disease, hypertension, and stroke.MethodsThis was a prospective cohort study, and the data was obtained from the China Health and Retirement Longitudinal Survey (CHARLS) implemented during 2011-2018 and the China Family Panel Studies (CFPS) implemented during 2010-2018. We applied a Cox proportional hazards regression model to evaluate the associations of MDA8 O3 with total CVD, heart disease, hypertension, and stroke risks, and the corresponding population-attributable fractions (PAF) attributable to MDA8 O3 were also calculated. All analyses were conducted by R software.ResultsThe mean MDA8 O3 concertation of all included participants in the CHARLS and CFPS were 51.03 part per billion (ppb) and 51.15 ppb, respectively. In the CHARLS including 18,177 participants, each 10 ppb increment in MDA8 O3 concentration was associated with a 31% increase [hazard ratio (HR) = 1.31, 95% confidence interval (CI): 1.22-1.42] in the risk of incident heart disease, and the corresponding population-attributable fractions (PAF) was 13.79% [10.12%-17.32%]. In the CFPS including 30,226 participants, each 10 ppb increment in MDA8 O3 concentration was associated with an increase in the risk of incident total CVD (1.07 [1.02-1.13]), and hypertension (1.10 [1.03-1.18]). The PAFs of total CVD, and hypertension attributable to MDA8 O3 were 3.53% [0.82%-6.16%], and 5.11% [1.73%-8.38%], respectively. Stratified analyses showed greater associations in males, urban areas, and Southern China.ConclusionsLong-term exposure to MDA8 O3 may increase the incidence of CVD. Therefore, the policies that control O3 and related precursors are persistently needed.
| S-EPMC11331174 | biostudies-literature
Project description:ImportanceFew studies have investigated the association of long-term ambient ozone exposures with respiratory morbidity among individuals with a heavy smoking history.ObjectiveTo investigate the association of historical ozone exposure with risk of chronic obstructive pulmonary disease (COPD), computed tomography (CT) scan measures of respiratory disease, patient-reported outcomes, disease severity, and exacerbations in smokers with or at risk for COPD.Design, setting, and participantsThis multicenter cross-sectional study, conducted from November 1, 2010, to July 31, 2018, obtained data from the Air Pollution Study, an ancillary study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). Data analyzed were from participants enrolled at 7 (New York City, New York; Baltimore, Maryland; Los Angeles, California; Ann Arbor, Michigan; San Francisco, California; Salt Lake City, Utah; and Winston-Salem, North Carolina) of the 12 SPIROMICS clinical sites. Included participants had historical ozone exposure data (n = 1874), were either current or former smokers (≥20 pack-years), were with or without COPD, and were aged 40 to 80 years at baseline. Healthy persons with a smoking history of 1 or more pack-years were excluded from the present analysis.ExposuresThe 10-year mean historical ambient ozone concentration at participants' residences estimated by cohort-specific spatiotemporal modeling.Main outcomes and measuresSpirometry-confirmed COPD, chronic bronchitis diagnosis, CT scan measures (emphysema, air trapping, and airway wall thickness), 6-minute walk test, modified Medical Research Council (mMRC) Dyspnea Scale, COPD Assessment Test (CAT), St. George's Respiratory Questionnaire (SGRQ), postbronchodilator forced expiratory volume in the first second of expiration (FEV1) % predicted, and self-report of exacerbations in the 12 months before SPIROMICS enrollment, adjusted for demographics, smoking, and job exposure.ResultsA total of 1874 SPIROMICS participants were analyzed (mean [SD] age, 64.5 [8.8] years; 1479 [78.9%] white; and 1013 [54.1%] male). In adjusted analysis, a 5-ppb (parts per billion) increase in ozone concentration was associated with a greater percentage of emphysema (β = 0.94; 95% CI, 0.25-1.64; P = .007) and percentage of air trapping (β = 1.60; 95% CI, 0.16-3.04; P = .03); worse scores for the mMRC Dyspnea Scale (β = 0.10; 95% CI, 0.03-0.17; P = .008), CAT (β = 0.65; 95% CI, 0.05-1.26; P = .04), and SGRQ (β = 1.47; 95% CI, 0.01-2.93; P = .048); lower FEV1% predicted value (β = -2.50; 95% CI, -4.42 to -0.59; P = .01); and higher odds of any exacerbation (odds ratio [OR], 1.37; 95% CI, 1.12-1.66; P = .002) and severe exacerbation (OR, 1.37; 95% CI, 1.07-1.76; P = .01). No association was found between historical ozone exposure and chronic bronchitis, COPD, airway wall thickness, or 6-minute walk test result.Conclusions and relevanceThis study found that long-term historical ozone exposure was associated with reduced lung function, greater emphysema and air trapping on CT scan, worse patient-reported outcomes, and increased respiratory exacerbations for individuals with a history of heavy smoking. The association between ozone exposure and adverse respiratory outcomes suggests the need for continued reevaluation of ambient pollution standards that are designed to protect the most vulnerable members of the US population.
| S-EPMC6902160 | biostudies-literature
Project description:BackgroundEpidemiologic studies on the effects of long-term exposure to ozone (O3) have shown inconclusive results. It is unclear whether to O3 has an effect on chronic kidney disease (CKD). We investigated the effects of O3 on mortality and renal outcome in CKD.MethodsWe included 61,073 participants and applied Cox proportional hazards models to examine the effects of ozone on the risk of end-stage renal disease (ESRD) and mortality in a two-pollutants model adjusted for socioeconomic status. We calculated the concentration of ozone exposure one year before enrollment and used inverse distance weighting (IDW) for interpolation, where the exposure was evenly distributed.ResultsIn the single pollutant model, O3 was significantly associated with an increased risk of ESRD and all-cause mortality. Based on the O3 concentration from IDW interpolation, this moving O3 average was significantly associated with an increased risk of ESRD and all-cause mortality. In a two-pollutants model, even after we adjusted for other measured pollutants, nitrogen dioxide did not attenuate the result for O3. The hazard ratio (HR) value for the district-level assessment is 1.025 with a 95% confidence interval (CI) of 1.014-1.035, while for the point-level assessment, the HR value is 1.04 with a 95% CI of 1.035-1.045. The impact of ozone on ESRD, hazard ratio (HR) values are, 1.049(95%CI: 1.044-1.054) at the district unit and 1.04 (95%CI: 1.031-1.05) at the individual address of the exposure assessment. The ozone hazard ratio for all-cause mortality was 1.012 (95% confidence interval: 1.008-1.017) for administrative districts and 1.04 (95% confidence interval: 1.031-1.05) for individual addresses.ConclusionsThis study suggests that long-term ambient O3 increases the risk of ESRD and mortality in CKD. The strategy to decrease O3 emissions will substantially benefit health and the environment.
| S-EPMC10900590 | biostudies-literature
Project description:BackgroundThe associations of long-term exposure to air pollutants in the presence of asthmatic symptoms remain inconclusive and the joint effects of air pollutants as a mixture are unclear.ObjectiveWe aimed to investigate the individual and joint associations of long-term exposure to ambient fine particulate matter (PM2.5) and daily 8-hour maximum ozone concentrations (MDA8 O3) in the presence of asthmatic symptoms in Chinese adults.MethodsData were derived from the World Health Organization Study on Global Ageing and Adult Health (WHO SAGE) cohort study among adults aged 50 years or older, which was implemented in 1 municipality and 7 provinces across China during 2007-2018. Annual average MDA8 O3 and PM2.5 at individual residential addresses were estimated by an iterative random forest model and a satellite-based spatiotemporal model, respectively. Participants who were diagnosed with asthma by a doctor or taking asthma-related therapies or experiencing related conditions within the past 12 months were recorded as having asthmatic symptoms. The individual associations of PM2.5 and MDA8 O3 with asthmatic symptoms were estimated by a Cox proportional hazards regression model, and the joint association was estimated by a quantile g-computation model. A series of subgroup analyses was applied to examine the potential modifications of some characteristics. We also calculated the population-attributable fraction (PAF) of asthmatic symptoms attributed to PM2.5 and MDA8 O3.ResultsA total of 8490 adults older than 50 years were included, and the average follow-up duration was 6.9 years. During the follow-up periods, 586 (6.9%) participants reported asthmatic symptoms. Individual effect analyses showed that the risk of asthmatic symptoms was positively associated with MDA8 O3 (hazard ratio [HR] 1.12, 95% CI 1.01-1.24, for per quantile) and PM2.5 (HR 1.18, 95% CI 1.05-1.31, for per quantile). Joint effect analyses showed that per equal quantile increment of MDA8 O3 and PM2.5 was associated with an 18% (HR 1.18, 95% CI 1.05-1.33) increase in the risk of asthmatic symptoms, and PM2.5 contributed more (68%) in the joint effects. The individual PAFs of asthmatic symptoms attributable to PM2.5 and MDA8 O3 were 2.86% (95% CI 0.17%-5.50%) and 4.83% (95% CI 1.42%-7.25%), respectively, while the joint PAF of asthmatic symptoms attributable to exposure mixture was 4.32% (95% CI 1.10%-7.46%). The joint associations were greater in participants with obesity, in urban areas, with lower family income, and who used unclean household cooking fuel.ConclusionsLong-term exposure to PM2.5 and MDA8 O3 may individually and jointly increase the risk of asthmatic symptoms, and the joint effects were smaller than the sum of individual effects. These findings informed the importance of joint associations of long-term exposure to air pollutants with asthma.
| S-EPMC10436124 | biostudies-literature
Project description: Not available
| S-EPMC6794103 | biostudies-literature
Project description:ObjectiveTo determine whether long term exposure to outdoor nitrogen dioxide (NO2) is associated with all-cause or cause-specific mortality.MethodsMEDLINE, Embase, CENTRAL, Global Health and Toxline databases were searched using terms developed by a librarian. Screening, data extraction and risk of bias assessment were completed independently by two reviewers. Conflicts were resolved through consensus and/or involvement of a third reviewer. Pooling of results across studies was conducted using random effects models, heterogeneity among included studies was assessed using Cochran's Q and I2 measures, and sources of heterogeneity were evaluated using meta-regression. Sensitivity of pooled estimates to individual studies was examined and publication bias was evaluated using Funnel plots, Begg's and Egger's tests, and trim and fill.ResultsSeventy-nine studies based on 47 cohorts, plus one set of pooled analyses of multiple European cohorts, met inclusion criteria. There was a consistently high degree of heterogeneity. After excluding studies with probably high or high risk of bias in the confounding domain (n = 12), pooled hazard ratios (HR) indicated that long term exposure to NO2 was significantly associated with mortality from all/ natural causes (pooled HR 1.047, 95% confidence interval (CI), 1.023-1.072 per 10 ppb), cardiovascular disease (pooled HR 1.058, 95%CI 1.026-1.091), lung cancer (pooled HR 1.083, 95%CI 1.041-1.126), respiratory disease (pooled HR 1.062, 95%CI1.035-1.089), and ischemic heart disease (pooled HR 1.111, 95%CI 1.079-1.144). Pooled estimates based on multi-pollutant models were consistently smaller than those from single pollutant models and mostly non-significant.ConclusionsFor all causes of death other than cerebrovascular disease, the overall quality of the evidence is moderate, and the strength of evidence is limited, while for cerebrovascular disease, overall quality is low and strength of evidence is inadequate. Important uncertainties remain, including potential confounding by co-pollutants or other concomitant exposures, and limited supporting mechanistic evidence. (PROSPERO registration number CRD42018084497).
| S-EPMC7861378 | biostudies-literature
Project description:BackgroundFew studies have assessed long-term effects of particulate matter (PM) with aerodynamic diameter < 2.5 μm (PM2.5) on mortality for causes of cancer other than the lung; we assessed the effects on multiple causes. In Hong Kong, most people live and work in urban or suburban areas with high-rise buildings. This facilitates the estimation of PM2.5 exposure of individuals, taking into account the height of residence above ground level for assessment of the long-term health effects with sufficient statistical power.MethodsWe recruited 66,820 persons who were ≥65 in 1998 to 2001 and followed up for mortality outcomes until 2011. Annual concentrations of PM at their residential addresses were estimated using PM2.5 concentrations measured at fixed-site monitors, horizontal-vertical locations, and satellite data. We used Cox regression model to assess the HR of mortality for cancer per 10 μg/m(3) increase of PM2.5 RESULTS: PM2.5 was associated with increased risk of mortality for all causes of cancer [HR, 1.22 (95% CI, 1.11-1.34)] and for specific cause of cancer in upper digestive tract [1.42 (1.06-1.89)], digestive accessory organs [1.35 (1.06-1.71)] in all subjects; breast [1.80 (1.26-2.55)] in females; and lung [1.36 (1.05-1.77)] in males.ConclusionsLong-term exposures to PM2.5 are associated with elevated risks of cancer in various organs.ImpactThis study is particularly timely in China, where compelling evidence is needed to support the pollution control policy to ameliorate the health damages associated with economic growth. Cancer Epidemiol Biomarkers Prev; 25(5); 839-45. ©2016 AACR.
| S-EPMC5505442 | biostudies-literature